Biomarkers of neurodegeneration in neural autoantibody-associated psychiatric syndromes: A retrospective cohort study

Neural Surface Antibodies and Neurodegeneration: Clinical Commonalities and Pathophysiological Relationships

“…Indeed, the two CSF biomarkers correlate with each other in AE [ 143 ]. On the other hand, while NFL levels are similar to those observed in AD [ 140 ], T-tau in AE is generally lower than in AD and the more AD-specific biomarker phosphorylated tau (P-tau181) is in most cases not increased [ 140 , 144 ]. Actually, in the large study of Day et al, on 45 cases of NSA-Ab positive AE (NSA-AE; NMDAR, LGI1 and CASPR2), after correction for age CSF levels of T-tau did not significantly differ from those of neurologically healthy controls (HC) [ 137 ].…”

“…Similarly, few studies have investigated CSF levels of amyloid β (Aβ) in AE. Although one study on AE patients (of whom not all had NSA-Ab) found a median CSF level of Aβ42 below the cut-off for AD [ 134 ], another investigation on AEs with antibodies (including some against ICAs) demonstrated lower CSF Aβ42 and lower CSF Aβ42/Aβ40 ratio compared to AD patients [ 144 ]. In a study on LGI1 encephalitis, almost one-third of patients had CSF levels of Aβ42 below the cut-off for AD; however, median CSF Aβ42 was higher compared to AD and similar to CJD and psychiatric patients, and no patient with LGI1 encephalitis had a true CSF AD profile (i.e., reduced Aβ42 along with increased T-tau and P-tau181) [ 140 ].…”